In the natural hearing process, ear anatomy mechanically translates sound into vibrations of the basilar membrane (BM) in the cochlea. These vibrations stimulate nerves connected to the spiral ganglion (SG) and, eventually, the auditory nerve. Researchers have extracted the tonotopic mapping between the frequency of the sound and the SG nerves that are stimulated, i.e., higher frequencies lead to stimulation of more basal SG nerves, whereas, lower frequencies stimulate more apical SG nerves [10].
Cochlear implants (CIs) are surgically implanted neural prosthetic devices used to treat severe-to-profound hearing loss [1]. CIs exploit the natural tonotopy by applying an electric field to more apical (basal) SG nerves to induce perceived lower (higher) frequency sounds. Over the last few decades, the design of CIs has evolved to produce what is arguably the most successful neural prosthesis to date. CIs induce hearing sensation by stimulating auditory nerve pathways within the cochlea using an implanted electrode array. The CI processor, typically worn behind the ear, is programmed to process sound received through a microphone and to send instructions to each electrode. CI programming begins with selection of a general signal processing strategy, e.g., continuous interleaved sampling [9]. Then, the audiologist defines what is referred to as the “MAP,” which is the set of CI processor instructions. The MAP is tuned by specifying stimulation levels for each electrode based on measures of the user's perceived loudness and by selecting a frequency allocation table, which defines which electrodes should be activated when specific frequencies are in the detected sound. The number of electrodes in the intracochlear array ranges from 12 to 22, depending on the manufacturer. Electrode activation stimulates spiral ganglion (SG) nerves, the nerve pathways that branch to the cochlea from the auditory nerve (see FIG. 1).
CI devices available today lead to remarkable results in the vast majority of users with average postoperative sentence recognition reaching over 70% correct for unilaterally implanted recipients and over 80% correct for bilateral implant recipients [31]. Despite this success, a significant number of users receive marginal benefit, and restoration to normal fidelity is rare even among the best performers. This is due, in part, to several well-known issues with electrical stimulation that prevent CIs from accurately simulating natural acoustic hearing. Electrode interaction is an example of one such issue that, despite significant improvements made by advances in hardware and signal processing, remains challenging [4, 5]. In natural hearing, a nerve pathway is activated when the characteristic frequency associated with that pathway is present in the incoming sound. Neural pathways are tonotopically ordered by decreasing characteristic frequency along the length of the cochlea, and this precisely tuned spatial organization is well known (see FIG. 1c) [10]. CI electrode arrays are designed such that when placement is optimal, each electrode stimulates nerve pathways corresponding to a pre-defined frequency bandwidth [3]. However, in surgery, the CI electrode array is blindly threaded into the cochlea with its insertion path guided only by the walls of the spiral-shaped intra-cochlear cavities. Since the final positions of the electrodes are generally unknown, the only option when designing the MAP has been to assume the electrodes are optimally situated in the cochlea and use a default frequency allocation table. Because MAP efficacy is sensitive to sub-optimal electrode positioning [2, 3], which can lead to, e.g., electrode channel interactions [4, 5], more effective MAPS could be selected if the positions of the electrodes were known.
It is widely believed that the best hearing restoration outcome can be achieved by stimulating, for a particular sound, the nerves that naturally correspond to the spectrum of that sound. However, this is not currently possible due to the following limitations:
(1) The depth of the implanted array typically falls short of the apical position corresponding to the lowest perceived frequencies. Thus, the lowest frequency nerves are not stimulated, and a frequency shifting artifact is introduced, i.e., each electrode stimulates nerves that correspond to higher frequencies than the ones of the detected sound.
(2) Using the small number of electrodes in the CI array (i.e., 12 to 22) and due to their large size relative to individual nerves, limited spectral resolution is achievable, i.e., an electrode cannot target individual nerves, but rather stimulates nerves corresponding to a wide range of frequencies.
(3) Individual electrodes are positioned at variable depths and perimodiolar distances. Moreover, there has been no technology developed that allows accurate assessment of electrode position relative to stimulation targets in vivo. Depth discrepancies result in a frequency shift artifact. A larger distance to the SG leads to wider current spread from each electrode, further decreasing the spectral resolution.
Therefore, a heretofore unaddressed need exists in the art to address the aforementioned deficiencies and inadequacies.